Vascular cognitive impairment and Alzheimer’s disease: role of cerebral hypoperfusion and oxidative stress

2012 ◽  
Vol 385 (10) ◽  
pp. 953-959 ◽  
Author(s):  
Hyun Ah Kim ◽  
Alyson A. Miller ◽  
Grant R. Drummond ◽  
Amanda G. Thrift ◽  
Thiruma V. Arumugam ◽  
...  
2021 ◽  
Vol 22 (5) ◽  
pp. 2283
Author(s):  
Yu-Jung Cheng ◽  
Chieh-Hsin Lin ◽  
Hsien-Yuan Lane

Alzheimer’s disease (AD), the most common cause of dementia, is a progressive neurodegenerative disease. The number of AD cases has been rapidly growing worldwide. Several the related etiological hypotheses include atypical amyloid β (Aβ) deposition, neurofibrillary tangles of tau proteins inside neurons, disturbed neurotransmission, inflammation, and oxidative stress. During AD progression, aberrations in neurotransmission cause cognitive decline—the main symptom of AD. Here, we review the aberrant neurotransmission systems, including cholinergic, adrenergic, and glutamatergic network, and the interactions among these systems as they pertain to AD. We also discuss the key role of N-methyl-d-aspartate receptor (NMDAR) dysfunction in AD-associated cognitive impairment. Furthermore, we summarize the results of recent studies indicating that increasing glutamatergic neurotransmission through the alteration of NMDARs shows potential for treating cognitive decline in mild cognitive impairment or early stage AD. Future studies on the long-term efficiency of NMDA-enhancing strategies in the treatment of AD are warranted.


2008 ◽  
Vol 34 (2) ◽  
pp. 373-378 ◽  
Author(s):  
Sagrario Martín-Aragón ◽  
Paloma Bermejo-Bescós ◽  
Juana Benedí ◽  
Emanuela Felici ◽  
Pedro Gil ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Ioana-Miruna Balmuș ◽  
Stefan-Adrian Strungaru ◽  
Alin Ciobica ◽  
Mircea-Nicusor Nicoara ◽  
Romeo Dobrin ◽  
...  

Increased interest regarding the biometal mechanisms of action and the pathways in which they have regulatory roles was lately observed. Particularly, it was shown that biometal homeostasis dysregulation may lead to neurodegeneration including Alzheimer’s disease, Parkinson disease, or prion protein disease, since important molecular signaling mechanisms in brain functions implicate both oxidative stress and redox active biometals. Oxidative stress could be a result of a breakdown in metal-ion homeostasis which leads to abnormal metal protein chelation. In our previous work, we reported a strong correlation between Alzheimer’s disease and oxidative stress. Consequently, the aim of the present work was to evaluate some of the biometals’ levels (magnesium, manganese, and iron), the specific activity of some antioxidant enzymes (superoxide dismutase and glutathione peroxidase), and a common lipid peroxidation marker (malondialdehyde concentration), in mild cognitive impairment (n=15) and Alzheimer’s disease (n=15) patients, compared to age-matched healthy subjects (n=15). We found increased lipid peroxidation effects, low antioxidant defense, low magnesium and iron concentrations, and high manganese levels in mild cognitive impairment and Alzheimer’s disease patients, in a gradual manner. These data could be relevant for future association studies regarding the prediction of Alzheimer’s disease development risk or circling through stages by analyzing both active redox metals, oxidative stress markers, and the correlations in between.


Open Biology ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 200084 ◽  
Author(s):  
Gerald Veurink ◽  
George Perry ◽  
Sandeep Kumar Singh

The joint attack on the body by metabolic acidosis and oxidative stress suggests that treatment in degenerative diseases, including Alzheimer's disease (AD), may require a normalizing of extracellular and intracellular pH with simultaneous supplementation of an antioxidant combination cocktail at a sufficiently high dose. Evidence is also accumulating that combinations of antioxidants may be more effective, taking advantage of synergistic effects of appropriate antioxidants as well as a nutrient-rich diet to prevent and reverse AD. This review focuses on nutritional, nutraceutical and antioxidant treatments of AD, although they can also be used in other chronic degenerative and neurodegenerative diseases.


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